Coracoid bone block versus arthroscopic Bankart repair: a comparative paired study with 5-year follow-up.

INTRODUCTION AND HYPOTHESIS: The hypothesis of this study was that the rate of recurrence of anterior instability of the shoulder after arthroscopic Bankart repair with suture anchors is higher than after coracoid bone block (Latarjet procedure). MATERIALS AND METHODS: This continuous retrospective monocentric study included a cohort of patients who underwent surgery for post-traumatic recurrent antero-inferior instability (2004-2005): 51 patients who underwent an open Latarjet procedure were paired for age at surgery to 51 patients who underwent an arthroscopic Bankart repair. All patients were evaluated with a questionnaire and 50% were evaluated in a follow-up consultation with X-rays. Recurrent instability was defined by at least one episode of anterior dislocation or subluxation. RESULTS: Demographic data, soft tissue and bone lesions were statistically similar between the groups. At 5 years follow-up, the recurrence rate was 24% in the Bankart group and 12% in the Latarjet group (P=012). In the Bankart group, age under 25 years old (P=0.01), competitive sports after surgery (P=0.01), and glenoid erosion (P=0.02) were independent risk factors of recurrence. In the Latarjet group, five technical errors were identified out of six cases of recurrence. Fifteen of the 18 cases of recurrence did not undergo revision surgery because patients remained satisfied with their results. DISCUSSION AND CONCLUSIONS: At 5 years of follow-up, the rate of recurrent instability following arthroscopic Bankart repair was two times higher than that following the coracoid bone block procedure. Young patients who wish to practice a competitive sport or present with glenoid erosion are poor candidates for arthroscopic Bankart repair. The rate of recurrence is extremely high in unselected patients. The open Latarjet procedure results in a fairly high rate of recurrence due to technical errors. LEVEL OF EVIDENCE: Level IV (retrospective study).

Recession wedge trochleoplasty as an additional procedure in the surgical treatment of patellar instability with major trochlear dysplasia: early results.

INTRODUCTION: The importance of a dysplastic trochlea as a component of patellar instability has long been recognized. An original trochleoplasty technique consisting in retro-trochlear recession wedge osteotomy was described by Goutallier et al. The aim is not to fashion a groove but to reduce the bump without modifying patellofemoral congruence. PATIENTS AND METHODS: This retrospective study reports the operative technique and short-term outcomes of a consecutive case series of 17 patients (19 knees) who underwent recession wedge trochleoplasty for patellofemoral instability associated with severe trochlear dysplasia. Other contributing factors of patellar instability were also corrected as part of the surgical procedure: tibial tuberosity transfer (n=18), MPFL reconstruction (n=8). RESULTS: Minimum follow-up was 12 months (mean, 34 months; range, 12 to 71 months). The trochlear prominence was reduced from a mean 4.8mm (range, 0 to 8mm) to -0.8mm (range, -8 to 6mm). Patellar tilt was reduced from a mean 14° (range, 6° to 26°) to 6° (range, -1° to 24°). Two cases showed recurrent patellofemoral instability. Mean Kujala, KOOS and IKDC score were respectively 80 (± 17), 70 (± 18) and 67 (± 17) at last follow-up. Three patients required further operations, apart from removal of metal screws: arthroscopic arthrolysis for stiffness (n=1), revision for tibial tuberosity non-union (n=1), and supratrochlear exostosectomy (n=1). DISCUSSION: Recession wedge trochleoplasty is a feasible additional procedure addressing bony trochlear abnormality in the surgical treatment of patellar instability. Our attitude is to perform it never in isolation but associated to realignment of the extensor apparatus according to the à la carte surgery concept. It seems to be effective in preventing future patellar dislocation and reducing anterior knee pain in case of painful patellofemoral instability with a major dysplastic trochlea, or in revision cases when other realignment procedures have failed.

Surgical treatment of the boxer's fracture: transverse pinning versus intramedullary pinning.

The purpose of this study was to compare the surgical treatment of fractures of the little finger metacarpal neck, or "Boxer's" fractures, by transverse pinning and intramedullary pinning. Thirty-six patients with fracture of the neck of the fifth metacarpal were included in a prospective comparative randomised study. A palmar splint was applied for 1 week after both procedures. Patients began physiotherapy three times per week for 30 days. The patients were evaluated clinically six times after surgery, up to the 90th day, with X-ray assessment on days 8, 45 and 90. The study showed that intramedullary pinning gave better functional outcomes than transverse pinning, although the former was more technically demanding.

The major synovial targets of the rheumatoid arthritis-specific antifilaggrin autoantibodies are deiminated forms of the alpha- and beta-chains of fibrin.

IgG antifilaggrin autoantibodies (AFA) are the most specific serological markers of rheumatoid arthritis. In epithelial tissues, they recognize citrulline-bearing epitopes present on various molecular forms of (pro)filaggrin. Histological analysis of rheumatoid synovial membranes with an Ab to citrulline showed labeling of interstitial amorphous deposits and mononuclear cells of various types. Immunochemical analysis of exhaustive sequential extracts of the same tissues showed that they contain several deiminated (citrulline containing) proteins. Among them, two proteins, p64--78 and p55--61, present in urea-DTT and guanidine extracts, were shown by immunoblotting to be specifically targeted by AFA. By amino-terminal sequencing the proteins were identified as deiminated forms of the alpha- and beta-chains of fibrin, respectively. Their identity was confirmed using several Abs specific for the A alpha- and/or to the B beta-chain of fibrin(ogen). Moreover, AFA-positive rheumatoid arthritis (RA) sera and purified AFA were highly reactive to the A alpha- and B beta-chains of human fibrinogen only after deimination of the molecules by a peptidylarginine deiminase. Autoantibodies affinity purified from a pool of RA sera onto deiminated fibrinogen were reactive toward all of the epithelial and synovial targets of AFA. This confirmed that the autoantibodies to the deiminated A alpha-and B beta-chains of fibrinogen, the autoantibodies to the synovial proteins p64--78 and p55--61, and, lastly, AFA, constitute largely overlapping autoantibody populations. These results show that deiminated forms of fibrin deposited in the rheumatoid synovial membranes are the major target of AFA. They suggest that autoimmunization against deiminated fibrin is a critical step in RA pathogenesis.

In the rheumatoid pannus, anti-filaggrin autoantibodies are produced by local plasma cells and constitute a higher proportion of IgG than in synovial fluid and serum.

IgG anti-filaggrin autoantibodies (AFA) are the most specific serological markers of rheumatoid arthritis (RA). They include the so-called 'anti-keratin antibodies' (AKA) and anti-perinuclear factor (APF), and recognize human epidermal filaggrin and other (pro)filaggrin-related proteins of various epithelial tissues. In this study we demonstrate that AFA are produced in rheumatoid synovial joints. In 31 RA patients, AFA levels were assayed at equal IgG concentrations in paired synovial fluids (SF) and sera. AFA titre-like values determined by indirect immunofluorescence and immunoblotting and AFA concentrations determined by ELISA were non-significantly different in serum and SF, clearly indicating that AFA are not concentrated in SF. In contrast, we demonstrated that AFA are enriched in RA synovial membranes, since the ELISA-determined AFA in low ionic-strength extracts of synovial tissue from four RA patients represented a 7.5-fold higher proportion of total IgG than in paired sera. When small synovial tissue explants from RA patients were cultured for a period of 5 weeks, the profile of IgG and AFA released in the culture supernatants was first consistent with passive diffusion of the tissue-infiltrating IgG (including AFA) over the first day of culture, then with a de novo synthesis of IgG and AFA. Therefore, AFA-secreting plasma cells are present in the synovial tissue of RA patients and AFA can represent a significant proportion of the IgG secreted within the rheumatoid pannus.

Anti-perinuclear factor compared with the so called "antikeratin" antibodies and antibodies to human epidermis filaggrin, in the diagnosis of arthritides.

OBJECTIVE: Antiperinuclear factor (APF), "antikeratin antibodies" ("AKA"), and antibodies to human epidermis filaggrin (AFA), are highly specific serological markers of rheumatoid arthritis (RA), which recognise epitopes on various isoforms of (pro)filaggrin. It was proposed that these antibodies are globally named antifilaggrin autoantibodies. Here the diagnostic value of the detection of each one is compared and the overlap between the three tests evaluated. METHODS: 492 serum samples were tested, including 279 RA serum samples, taken from patients in France and Belgium. APF and "AKA" titres were estimated by indirect immunofluorescence, and AFA titres by immunoblotting on filaggrin enriched human epidermis extracts. RESULTS: By a convenient choice of the positivity thresholds, the diagnostic sensitivity and specificity of the tests were shown to be similar (0.52 and 0.97, respectively). Although the antibody titres were strongly correlated, the associations APF-AFA or AFA-"AKA" permitted more than 52% or 55% of RA to be diagnosed, with a specificity of 0.99. CONCLUSION: APF, "AKA", and AFA detection have a similar diagnostic value. However, because the three tests do not totally overlap, associating APF with "AKA" or AFA with "AKA" can improve diagnostic sensitivity. None of the three antigens used bear all the epitopes recognised by antifilaggrin autoantibodies.

The epitopes targeted by the rheumatoid arthritis-associated antifilaggrin autoantibodies are posttranslationally generated on various sites of (pro)filaggrin by deimination of arginine residues.

Antifilaggrin autoantibodies (AFA) are a population of IgG autoantibodies associated to rheumatoid arthritis (RA), which includes the so-called "antikeratin" Abs and antiperinuclear factor. AFA are the most specific serological markers of RA. We previously showed that they recognize human epidermal filaggrin and other profilaggrin-related proteins of various epithelial tissues. Here, we report further characterization of the protein Ags and epitopes targeted by AFA. All the Ags that exhibit numerous neutral/ acidic isoelectric variants were immunochemically demonstrated to be deiminated proteins. In vitro deimination of a recombinant human filaggrin by a peptidylarginine deiminase generated AFA epitopes on the protein. Moreover, two of three filaggrin-derived synthetic peptides with a citrulline in the central position were specifically and widely recognized by AFA affinity-purified from a series of RA sera. These results indicate that citrulline residues are constitutive of the AFA epitopes, but only in the context of specific amino acid sequences of filaggrin. In competition experiments, the two peptides abolished the AFA reactivity of RA sera, showing that they present major AFA epitopes. These data should help in the identification of a putative deiminated AFA-inducing or cross-reactive articular autoantigen and provide new insights into the pathogenesis of RA. They could also open the way toward specific immunosuppressive and/or preventive therapy of RA.

The antiperinuclear factor and the so-called antikeratin antibodies are the same rheumatoid arthritis-specific autoantibodies.

The so-called antikeratin antibodies (AKA) and the antiperinuclear factor (APF) are the most specific serological markers of RA. Using indirect immunofluorescence, AKA label the stratum corneum of various cornified epithelia and APF the keratohyalin granules of human buccal mucosa epithelium. We recently demonstrated that AKA recognize human epidermal filaggrin. Here, we report the identification of the major APF antigen as a diffuse protein band of 200-400 kD. This protein is seen to be closely related to human epidermal (pro) filaggrin since it was recognized by four antifilaggrin mAbs specific for different epitopes, and since the APF titers of RA sera were found to be correlated to their AKA titers and to their immunoblotting reactivities to filaggrin. Immunoabsorption of RA sera on purified epidermal filaggrin abolished their reactivities to the granules of buccal epithelial cells and to the 200-400-kD antigen. Moreover, antifilaggrin autoantibodies, i.e., AKA, affinity purified from RA sera, were shown to immunodetect the 200-400-kD antigen and to stain these granules. These results indicate that AKA and APF are largely the same autoantibodies. They recognize human epidermal filaggrin and (pro) filaggrin-related proteins of buccal epithelial cells. Identification of the epitopes recognized by these autoantibodies, which we propose to name antifilaggrin autoantibodies, will certainly open new paths of research into the pathophysiology of RA.